Imaging of the Aortic Valve Using Fluorodeoxyglucose Positron Emission Tomography: Increased Valvular Fluorodeoxyglucose Uptake in Aortic Stenosis
Is aortic stenosis (AS) associated with evidence of valvular inflammation based on fluorodeoxyglucose uptake on positron emission tomography (FDG-PET)?
FDG-PET/computed tomography data were retrospectively evaluated in 84 patients (ages 73 ± 9 years, 45% women), including 42 patients with AS and 42 age-matched controls. FDG uptake was determined within the aortic valve (AV) while blinded to AS severity. Target-to-background ratio was calculated as valvular/blood activity. Stenosis severity was established on echocardiography, and the presence of AV calcification was independently assessed on computed tomography.
The AV PET signal was increased in AS compared with controls: (median 1.53, interquartile range [IQR] 1.42-1.76 vs. median 1.34, IQR 1.20-1.55; p < 0.001). Compared with controls, AV PET was increased in mild (median 1.50, IQR 1.36-1.75; p = 0.01) and moderate (median 1.70, IQR 1.52-1.94; p < 0.001), but not in severe AS (median 1.49, IQR 1.40-1.54; p = 0.08). When subjects were categorized according to AV calcification and compared with noncalcified valves (median 1.35, IQR 1.20-1.52), valvular FDG uptake was increased in mildly (median 1.50, IQR 1.36-1.79; p < 0.01) and moderately (median 1.67, IQR 1.50-1.85; p < 0.001), but not severely calcified valves (median 1.51, IQR 1.381.54; p = 0.15).
This study supports the hypothesis that AS is an inflammatory condition, and suggests that inflammation may be reduced in late-stage disease. This may have important implications in the design of studies assessing the effect of therapeutic agents in modifying progression of AS.
Degenerative calcific AS currently is thought to result from active proliferative and inflammatory changes, with lipid accumulation, up-regulation of angiotensin-converting enzyme activity, and infiltration of macrophages and T-lymphocytes, ultimately leading to calcium deposition similar to other vascular calcification. Although direct clinical data are lacking, this study provides data from FDG uptake on PET that supports the role of local inflammation within the AV in the progression of AS. Notably, although inflammation appeared to be increased in earlier stages of AS, it was not in patients with more advanced disease. This might explain why earlier studies have failed to show an impact of therapy to delay the progression of AS; therapy might be effective only before calcification and stenosis progress to a clinically significant stage. As with coronary artery atherosclerosis, degenerative calcific AS might best be targeted using efforts at primary prevention among patients at risk.
Keywords: Inflammation, Fluorodeoxyglucose F18, Atherosclerosis, Tomography, X-Ray Computed, Coronary Vessels, Echocardiography, Positron-Emission Tomography
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